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Practice EssentialsUrinary tract infections (UTIs) are common in females, accounting for over 6 million patient visits to physicians per year in the United States. Cystitis (bladder infection) represents the majority of these infections (see the image below). Related terms include pyelonephritis, which refers to upper urinary tract infection; bacteriuria, which describes bacteria in the urine; and candiduria, which describes yeast in the urine. Plain radiograph in a 63-year-old patient with poorly controlled type 2 diabetes mellitus shows emphysematous cystitis.Signs and symptomsSymptoms and signs of UTI in the adult are as follows:
See Clinical Presentation for more detail. DiagnosisDiagnostic studies for UTI consist of dipstick, urinalysis, and culture. No imaging studies are indicated in the routine evaluation of cystitis. Current emphasis in the diagnosis of UTI rests with the detection of pyuria, as follows:
Other findings are as follows:
Urine culture remains the criterion standard for the diagnosis of UTI. Consider obtaining urine cultures in patients with probable cystitis if any of the following is present:
Definitions of UTI in women, based on culture results in clean-catch urine specimens, are as follows:
Any amount of uropathogen grown in culture from a suprapubic aspirate should be considered evidence of a UTI. See Workup for more detail. ManagementOral therapy with an empirically chosen antibiotic that is effective against gram-negative aerobic coliform bacteria (eg, Escherichia coli) is the principal treatment intervention in patients with cystitis. The first-choice agents for treatment of uncomplicated acute cystitis in women include the following:
Considerations in antibiotic selection are as follows:
Duration of antibiotic treatment for acute, uncomplicated cystitis in women who are not pregnant is as follows:
The vast majority of women with UTI present on an ambulatory basis and can be treated as outpatients. Hospital admission may be indicated for some patients with complicated UTI. Complicating factors include the following:
See Treatment and Medication for more detail. BackgroundUrinary tract infections (UTIs) are common in females, and cystitis (bladder infection) represents the majority of these infections. Related terms include pyelonephritis, which refers to upper urinary tract infection; bacteriuria, which describes bacteria in the urine; and candiduria, which describes yeast in the urine. Very ill patients may be referred to as having urosepsis. UTI is defined as significant bacteriuria in the setting of symptoms of cystitis or pyelonephritis. These infections account for a significant number of emergency department (ED) visits, [3] and 20% of women develop at least one UTI. (See Epidemiology.) Escherichia coli causes the majority of uncomplicated cystitis cases. Among the pathogens responsible for the remainder are Staphylococcus saprophyticus, Proteus mirabilis, Klebsiella pneumonia e, or Enterococcus faecalis. (See Etiology.) A presumptive diagnosis of uncomplicated cystitis can be made on the basis of findings on the history and physical examination, along with urinalysis. [4, 5] Proper specimen collection is necessary. In addition, clinicians need to appreciate the epidemiological and host factors that may identify patients with complicated cystitis or clinically inapparent upper UTI, in whom more comprehensive assessment is indicated. (See Workup.) Successful emergent management includes selection of appropriate antimicrobial therapy with recommendations for follow-up care. Oral therapy with an antibiotic effective against gram-negative aerobic coliform bacteria is the principal therapeutic intervention in patients with cystitis. (See Treatment, as well as Medication.) The following terms are defined for uniformity in this article:
PathophysiologyThe urinary tract is normally sterile. Uncomplicated UTI involves the urinary bladder in a host without underlying renal, metabolic, or neurologic diseases. Cystitis represents bladder mucosal invasion, most often by enteric coliform bacteria (eg, Escherichia coli) that inhabit the periurethral vaginal introitus and ascend into the bladder via the urethra. In recurrent E coli UTIs, peak colonization rates of the periurethral area 2-3 days prior to the development of the symptoms of acute cystitis range from 46-90%. During this same period, asymptomatic bacteriuria rates increase from 7% to 70%. [6] Because sexual intercourse may promote this migration, cystitis is common in otherwise healthy young women. Generally, urine is a good culture medium. Factors unfavorable to bacterial growth include a low pH (5.5 or less), a high concentration of urea, and the presence of organic acids derived from a diet that includes fruits and protein. Organic acids enhance acidification of the urine. Frequent and complete voiding has been associated with a reduction in the incidence of UTI. Normally, a thin film of urine remains in the bladder after emptying, and any bacteria present are removed by the mucosal cell production of organic acids. If the defense mechanisms of the lower urinary tract fail, upper tract or kidney involvement occurs and is termed pyelonephritis. Host defenses at this level include local leukocyte phagocytosis and renal production of antibodies that kill bacteria in the presence of complement. For more information on this topic, see the Medscape Reference articles Acute Pyelonephritis and Pathophysiology of Complicated Urinary Tract Infections. In general, there are 3 main mechanisms responsible for UTIs:
Bacterial virulenceUropathogenic bacteria, derived from a subset of fecal flora, have traits that enable adherence, growth, and resistance of host defenses. These traits facilitate colonization and infection of the urinary tract. Adhesins are bacterial surface structures that enable attachment to host membranes. In E coli infection, these include both pili (ie, fimbriae) and outer-membrane proteins (eg, Dr hemagglutinin). P fimbriae , which attach to globoseries-type glycolipids found in the colon and urinary epithelium, are associated with pyelonephritis and cystitis and are found in many E coli strains that cause urosepsis. Type 1 fimbriae bind to mannose-containing structures found in many different cell types, including Tamm-Horsfall protein (the major protein found in human urine). Whether this facilitates or inhibits uroepithelial colonization is the subject of some debate. Other factors that may be important for E coli virulence in the urinary tract include capsular polysaccharides, hemolysins, cytotoxic necrotizing factor (CNF) protein, and aerobactins. Several Kauffman serogroups of E coli that contain these virulence factors may be more likely to cause UTIs, including O1, O2, O4, O6, O16, and O18. Another example of bacterial virulence is the swarming capability of Proteus mirabilis. Swarming involves the expression of specific genes when these bacteria are exposed to surfaces such as catheters. This results in the coordinated movement of large numbers of bacteria, enabling P mirabilis to move across solid surfaces. This likely explains the association of P mirabilis UTIs with instrumentation of the urinary tract. Host resistanceMost uropathogens gain access to the urinary tract via an ascending route. The shorter length of the female urethra allows uropathogens easier access to the bladder. The continuous unidirectional flow of urine helps to minimize UTIs, and anything that interferes with this increases the host's susceptibility to UTI. Examples of interference include volume depletion, sexual intercourse, urinary tract obstruction, instrumentation, use of catheters not drained to gravity, and vesicoureteral reflux. Secretory defenses help promote bacterial clearance and prevent adherence. Secretory immunoglobulin A (IgA) reduces attachment and invasion of bacteria in the urinary tract. Women who are nonsecretors of the ABH blood antigens appear to be at higher risk for recurrent UTIs; this may occur because of a lack of specific glycosyltransferases that modify epithelial surface glycolipids, allowing E coli to bind to them better. In premenopausal women, lactobacilli are the predominant vaginal flora and serve to suppress vaginal colonization by the uropathogens. Most antibiotics, except sulfamethoxazole and the quinolones, can eradicate these protective bacteria. Urine itself has several antibacterial features that suppress UTIs. Specifically, the pH, urea concentration, osmolarity, and various organic acids prevent most bacteria from surviving in the urinary tract. EtiologyE coli causes 70-95% of both upper and lower UTIs. Various organisms are responsible for the remainder of infections, including S saprophyticus, Proteus species, Klebsiella species, Enterococcus faecalis, other Enterobacteriaceae, and yeast. Some species are more common in certain subgroups, such as Staphylococcus saprophyticus in young women. However, S saprophyticus can produce acute cystitis in older women and in young men and should not be automatically regarded as a contaminant in the urine cultures of these individuals. [7] Most complicated UTIs are nosocomial in origin. Increasingly, UTIs in patients in health care institutions and in those with frequent antibiotic exposure are caused by multidrug-resistant gram-negative pathogens, such as extended-spectrum beta-lactamase (ESBL) and carbapenemase producers. However, the prevalence of multidrug-resistant pathogens varies by locale. [8] The most important risk factor for bacteriuria is the presence of a catheter. [9] Eighty percent of nosocomial UTIs are related to urethral catheterization, while 5-10% are related to genitourinary manipulation. Catheters inoculate organisms into the bladder and promote colonization by providing a surface for bacterial adhesion and causing mucosal irritation. For more information on this topic, see the Medscape Reference article Catheter-Related Urinary Tract Infection. Sexual intercourse contributes to increased risk, as does use of a diaphragm and/or spermicide. Routine pelvic examinations are also associated with an increased risk of a UTI for 7 weeks post procedure. [10] Women who are elderly, are pregnant, or have preexisting urinary tract structural abnormalities or obstruction carry a higher risk of UTI. UTIs are the most common type of infection following renal transplantation. Susceptibility is especially high in the first 2 months following transplantation. Triggering factors include vesicoureteral reflux and immunosuppression. Corynebacterium urealyticum (ie, CDC group D2) has been reported to cause encrusted pyelitis and cystitis in these patients. Calculi related to UTIs most commonly occur in women who experience recurrent UTIs with Proteus, Pseudomonas, and Providencia species. Perinephric abscesses are associated most commonly with E coli, Proteus species, and S aureus but also may be secondary to Enterobacter, Citrobacter, Serratia, Pseudomonas, and Klebsiella species. More unusual causes include enterococci, Candida species, anaerobes, Actinomyces species, and Mycobacterium tuberculosis. Twenty-five percent of infections are polymicrobial. Candiduria is defined as more than 1000 CFU/mL of yeast from 2 cultures. Candida albicans, which is germ tube positive, is the usual culprit. Germ tube–negative Candida species (tropicalis, parapsilosis, glabrata, lusitaniae, krusei) are less common. Risk factors for candiduria include diabetes mellitus, indwelling urinary catheters, and antibiotic use. Candiduria may clear spontaneously or may result in (or from) deep fungal infections. EpidemiologyUnited States statisticsUTIs in women are very common; approximately 25-40% of women in the United States aged 20-40 years have had a UTI. UTIs account for over 6 million patient visits to physicians per year in the United States. Approximately 20% of those visits are to EDs. Cystitis occurs in 0.3-1.3% of pregnancies but does not appear to be related to asymptomatic bacteriuria. Acute pyelonephritis occurs in 1-2% of pregnancies. UTIs occur in 30-50% of renal transplant patients and frequently are silent. In 2007, approximately 3.9% of office visits were related to symptoms involving the genitourinary tract. [11] Estimates based on office and ED visits suggest per annum about 7 million episodes of acute cystitis. Some studies estimate that UTIs (cystitis plus pyelonephritis) cost at least $1 billion per year. International statisticsUTIs have been well studied in Sweden and other parts of Europe. [12] These studies have shown that 1 in 5 adult women experience a UTI at some point, confirming that it is an exceedingly common worldwide problem. The epidemiology of UTI in the tropics is less well documented. UTIs appear to be common and associated with structural abnormalities. Chronic infection from Schistosoma haematobium disrupts bladder mucosal integrity and causes urinary tract obstruction and stasis. Salmonella bacteriuria, with or without bacteremia, is very common in patients with schistosomiasis. Treatment requires both antischistosomal and anti-Salmonella agents. Age- and sex-related demographicsUncomplicated UTIs are much more common in women than men when matched for age. A study of Norwegian men aged 21-50 years showed an approximate incidence of 0.0006-0.0008 infections per person-year, compared with approximately 0.5-0.7 per person-year in similarly aged women in the United States. The largest group of patients with UTI is adult women. The incidence of UTI in women tends to increase with increasing age. Several peaks above baseline correspond with specific events, including an increase in women aged 18-30 years (associated with coitus—so-called honeymoon cystitis—and pregnancy). Rates of infection are high in postmenopausal women because of bladder or uterine prolapse causing incomplete bladder emptying; loss of estrogen with attendant changes in vaginal flora (notably, loss of lactobacilli), which allows periurethral colonization with gram-negative aerobes, such as E coli; and higher likelihood of concomitant medical illness, such as diabetes. Of neonates, boys are slightly more likely than girls to present with UTI as part of a gram-negative sepsis syndrome. The incidence in preschool-aged children is approximately 2% and is 10 times more common in girls. UTI occurs in 5% of school-aged girls, but it is rare in school-aged boys. Prognosis
Even with effective antibiotic treatment, the average duration of severe symptoms in women with cystitis is somewhat longer than 3 days. Features that have been associated with a more prolonged course than average include a history of somatization, previous cystitis, urinary frequency, and more severe symptoms at baseline. [13] . Although simple lower UTI (cystitis) may resolve spontaneously, effective treatment lessens the duration of symptoms and reduces the incidence of progression to upper UTI. Even with effective treatment, however, about 25% of women with cystitis will experience a recurrence. Younger patients have the lowest rates of morbidity and mortality. Factors associated with an unfavorable prognosis include the following:
The mortality associated with acute uncomplicated cystitis in women aged 20-60 years appears to be negligible. A longitudinal cohort study of Swedish women showed a higher mortality in women with a history of UTI than in age-matched women without such a history (37% versus 28% in 10 y), [14] but these cohorts were not matched for other mortality-related factors, making it difficult to attribute the increased mortality to UTIs. In contrast, the morbidity in terms of quality of life and economic measures is tremendous. Each episode of UTI in a young woman results in an average of 6.1 days of symptoms, 1.2 days of decreased class/work attendance, and 0.4 days in bed. Nosocomial infections develop in about 5% of patients admitted to hospitals, and UTIs account for 40% of these infections. From 2-4% of these patients become bacteremic, with a mortality of 12.5%. Patient EducationProper adherence to the outpatient medical regimen should be stressed. Behavior modification, such as good oral fluid intake to enhance diuresis and frequent voiding (including postintercourse voiding) may be helpful in reducing recurrent infection. (See Prevention of Urinary Tract Infections.) For patient education information, see the Infections Center, as well as Urinary Tract Infection (UTI), Blood in the Urine, Birth Control Overview, Birth Control Spermicides, and Birth Control FAQs.
Author Coauthor(s) Chief Editor Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America; Fellow of the Royal College of Physicians, London Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Medical Association, Association of Professors of Medicine, Infectious Diseases Society of America, Oklahoma State Medical Association, Southern Society for Clinical Investigation Disclosure: Nothing to disclose. Additional Contributors Acknowledgements Michael S Beeson, MD, MBA, FACEP Professor of Emergency Medicine, Northeastern Ohio Universities College of Medicine and Pharmacy; Attending Faculty, Akron General Medical Center Michael S Beeson, MD, MBA, FACEP is a member of the following medical societies: American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, National Association of EMS Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Pamela L Dyne, MD Professor of Clinical Medicine/Emergency Medicine, University of California, Los Angeles, David Geffen School of Medicine; Attending Physician, Department of Emergency Medicine, Olive View-UCLA Medical Center Pamela L Dyne, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. David S Howes, MD Professor of Medicine and Pediatrics, Section Chief and Emergency Medicine Residency Program Director, University of Chicago Division of the Biological Sciences, The Pritzker School of Medicine David S Howes, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Physicians-American Society of Internal Medicine, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Elicia S Kennedy, MD Clinical Assistant Professor, Department of Emergency Medicine, University of Arkansas for Medical Sciences Elicia S Kennedy, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Klaus-Dieter Lessnau, MD, FCCP Clinical Associate Professor of Medicine, New York University School of Medicine; Medical Director, Pulmonary Physiology Laboratory; Director of Research in Pulmonary Medicine, Department of Medicine, Section of Pulmonary Medicine, Lenox Hill Hospital Klaus-Dieter Lessnau, MD, FCCP is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, American Medical Association, American Thoracic Society, and Society of Critical Care Medicine Disclosure: Sepracor None None Allison M Loynd, DO Resident Physician, Department of Emergency Medicine, Wayne State University School of Medicine, Detroit Receiving Hospital Allison M Loynd, DO is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, and Emergency Medicine Residents Association Disclosure: Nothing to disclose. Mark Jeffrey Noble, MD Consulting Staff, Urologic Institute, Cleveland Clinic Foundation Mark Jeffrey Noble, MD is a member of the following medical societies: American College of Surgeons, American Medical Association, American Urological Association, Kansas Medical Society, Sigma Xi, Society of University Urologists, and Southwest Oncology Group Disclosure: Nothing to disclose. Adam J Rosh, MD Assistant Professor, Department of Emergency Medicine, Detroit Receiving Hospital, Wayne State University School of Medicine Adam J Rosh, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Joseph A Salomone III, MD Associate Professor and Attending Staff, Truman Medical Centers, University of Missouri-Kansas City School of Medicine; EMS Medical Director, Kansas City, Missouri Joseph A Salomone III, MD is a member of the following medical societies: American Academy of Emergency Medicine, National Association of EMS Physicians, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Richard H Sinert, DO Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Disclosure: Medscape Salary Employment Mark Zwanger, MD, MBA Assistant Professor, Department of Emergency Medicine, Jefferson Medical College of Thomas Jefferson University Mark Zwanger, MD, MBA is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, and American Medical Association Disclosure: Nothing to disclose. What types of bacteria cause urinary tract infections?The most common bacteria found to cause UTIs is Escherichia coli (E. coli). Other bacteria can cause UTI, but E. coli is the culprit about 90 percent of the time.
Which bacteria is the most common cause of urinary tract infections?UTIs in Women
E. coli bacteria, which live in the bowel, cause most UTIs.
What types of bacteria are found in urine?Escherichia coli strains are the most common isolate, founded in 80%of the urine samples of patients with a simple UTI (cystitis), followed by Staphylococcus saprophyticus (5-15%), whereas Klebsiella, Enterobacter or Proteus rarely cause infection outside the hospital (5- 10%) (6).
What are the 8 most common causes of UTIs?Here are 8 of the most common causes of urinary tract infections—and a handful of helpful tips for prevention.. Sex. We know, huge bummer. ... . Constipation. You might be able to blame your poop (or lack thereof) for your UTI. ... . Uncontrolled diabetes. ... . Holding it. ... . Dehydration. ... . Birth control. ... . Feminine products. ... . Kidney stones.. |